ArticleAmerican journal of physiology. Heart and circulatory physiology2016
Spontaneous initiation of premature ventricular complexes and arrhythmias in type 2 long QT syndrome.
Article in American journal of physiology. Heart and circulatory physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 46 citations in OpenAlex.
- Phase 2 Re-Entry Without IJACC. Clinical electrophysiology · 2023Trial
- Variable expressivity in long QT syndrome type 2 rabbits defines a low threshold for therapeuticAmerican journal of physiology. Heart and circulatory physiology · 2026Article
- Modes of onset of ventricular arrhythmias in J-wave syndromes: mechanistic insights from computational modeling.American journal of physiology. Heart and circulatory physiology · 2026Article
- Are physiological oscillations physiological?The Journal of physiology · 2026Review
- Ventricular Arrhythmias Associated With Long QT Syndrome Type 2 and Anomalous Right Coronary Artery.JACC. Case reports · 2026Article
- Population Modeling Approach for Human Cardiac Arrhythmia Risk Prediction.Circulation. Arrhythmia and electrophysiology · 2026Article
- Methadone Blockade of Inward Rectifier Potassium Current Promotes Both Early and Delayed Repolarization Arrhythmias: Mechanistic Insights From Computational Modeling.Journal of the American Heart Association · 2025Article
- Arrhythmic events pertinent with antidepressants: a Bayesian disproportional analysis mining the FDA Adverse Event Reporting System database.Frontiers in psychiatry · 2025Article
- Curvature-mediated source and sink effects on the genesis of premature ventricular complexes in long QT syndrome.American journal of physiology. Heart and circulatory physiology · 2024Article
- Intracellular ion accumulation in the genesis of complex action potential dynamics under cardiac diseases.Physical review. E · 2024Article
- Dissecting the roles of calcium cycling and its coupling with voltage in the genesis of early afterdepolarizations in cardiac myocyte models.PLoS computational biology · 2024Article
- Mechanisms of torsades de pointes: an update.Frontiers in cardiovascular medicine · 2024Review
- Heterogeneous cardiac sympathetic innervation gradients promote arrhythmogenesis in murine dilated cardiomyopathy.JCI insight · 2023Article
- Optogenetic Modulation of Arrhythmia Triggers: Proof-of-Concept from Computational Modeling.Cellular and molecular bioengineering · 2023Article
- Initiation of ventricular arrhythmia in the acquired long QT syndrome.Cardiovascular research · 2023Article
- Bifurcations to transient and oscillatory excitations in inhomogeneous excitable media: Insights into arrhythmogenesis in long QT syndrome.Physical review. E · 2023Article
- Mechanistic insights into spontaneous transition from cellular alternans to ventricular fibrillation.Physiological reports · 2023Article
- R-on-T and the initiation of reentry revisited: Integrating old and new concepts.Heart rhythm · 2022Article
- Triiodothyronine and dexamethasone alter potassium channel expression and promote electrophysiological maturation of human-induced pluripotent stem cell-derived cardiomyocytes.Journal of molecular and cellular cardiology · 2021Article
- Mechanisms of phase-3 early afterdepolarizations and triggered activities in ventricular myocyte models.Physiological reports · 2021Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
The occurrence of early afterdepolarizations (EADs) and increased dispersion of repolarization are two known factors for arrhythmogenesis in long QT syndrome. However, increased dispersion of repolarization tends to suppress EADs due to the source-sink effect, and thus how the two competing factors cause initiation of arrhythmias remains incompletely understood. Here we used optical mapping and computer simulation to investigate the mechanisms underlying spontaneous initiation of arrhythmias in type 2 long QT (LQT2) syndrome. In optical mapping experiments of transgenic LQT2 rabbit hearts under isoproterenol, premature ventricular complexes (PVCs) were observed to originate from the steep spatial repolarization gradient (RG) regions and propagated unidirectionally. The same PVC behaviors were demonstrated in computer simulations of tissue models of rabbits. Depending on the heterogeneities, these PVCs could lead to either repetitive focal excitations or reentry without requiring an additional vulnerable substrate. Systematic simulations showed that cellular phase 2 EADs were either suppressed or confined to the long action potential region due to the source-sink effect. Tissue-scale phase 3 EADs and PVCs occurred due to tissue-scale dynamical instabilities caused by RG and enhanced L-type calcium current (I
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.